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颈动脉注射肾上腺髓质素对去缓冲神经大鼠最后区神经元自发放电的影响(英文) 被引量:3

Effect of intracarotid administration of adrenomedullin on the spontaneous electrical activity of area postrema neurons in sino-aortic denervated rats
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摘要 在63只切断两侧缓冲神经的麻醉sprague-Dawley大鼠,应用细胞外记录的电生理学方法,观察颈内动脉注射肾上腺髓质素(adrenomedullin,AM)对最后区(area postrema,AP)神经元自发电活动的影响。实验结果如下:(1)在记录到的78个自发放电单位中,颈内动脉内注射AM(0.3 nmol/kg),引起其中47个单位的自发放电频率由2.99±0.24增加到4.79±0.29 spikes/s(P<0.001),20个单位自发放电频率由3.24±0.46下降至1.97±0.37 spikes/s(P<0.001),另外11个单位自发放电频率无明显改变;平均动脉压和心率无明显变化。(2)颈内动脉注射降钙素基因相关肽受体阻断剂CGRP_(8-37)(3 nmol/kg)不能改变AM对自发放电的兴奋效应;(3)颈内动脉注射L-精氨酸(30 mg/kg)可减弱AM对自发放电的兴奋效应。以上结果提示,AM对最后区神经元有兴奋作用,此作用不是由降钙素基因相关肽受体介导,但可被NO前体L-精氨酸所减弱。 To observe the effect of intracarotid administration of adrenomedullin (AM) on the spontaneous electrical activity of area postrema (AP) neurons, 78 spontaneous active units were recorded from 63 sino-aortic denervated Sprague-Dawley rats using extracellular recording technique. The results obtained are as follows. (1) Following intracarotid administration of AM (0.3 nmol/kg), the discharge rate of 47 out of 78 units increased markedly from 2.99±0.24 to 4.79±0.29 spikes/s (P<0.001), 20 units decreased from 3.24+0.46 to 1.97±0.37 spikes/s (P<0.001), and the remaining 11 showed no response.Blood pressure (BP) and heart rate (HR) did not change throughout the experimentation. (2) Pretreatment with intracarotid administration of caleitonin gene-related peptide receptor antagonist CGRP_(8-37) (3 nmol/kg) did not change the effects of AM. (3) Following intracarotid injection of NO precursor L-arginine (30mg/kg), the excitatory effect of AM was attenuated. The above results indicate that AM can excite spontaneous electrical activity of AP neurons, this effect is not mediated by calcitanin gene-related peptide receptor but may be attenuated by NO precursor L-arginine.
出处 《生理学报》 CAS CSCD 北大核心 2003年第4期395-400,共6页 Acta Physiologica Sinica
关键词 肾上腺髓质素 最后区 自发放电单位 降钙素基因相关肽受体拮抗剂 L-精氨酸 adrenomedullin area postrema spontaneous single-units discharge caicitonin gene-related peptide receptor antagonist L-arginine
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